A model of Bcl-2 family member control over programmed cell death. In response to myriad death, damage, or derangement signals, BH3-only family members are activated (i). Activator BH3-only proteins interact with multidomain proapoptotic Bax and/or Bak (Bax/Bak), inducing their oligomerization (ii) and thus resulting in MOMP, release of cytochrome c, apoptosome formation, and caspase activation (iii). Bcl-2 and other multidomain antiapoptotic proteins interrupt the death signal by binding and sequestering activator BH3-only family members, and perhaps also Bax/Bak (iv). Bcl-2 antiapoptotic function may be antagonized by the competitive displacement of activator BH3-only molecules by sensitizer BH3-only proteins (v).